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Superior Orbital Fissure Syndrome:

A Case Report
Heath H. Evans, D.D.S. 1

Bradley A. Wurth, D.M.D. 1

1 Oral and Maxillofacial Surgery, Nassau University Medical Center, East

Meadow, New York

Craniomaxillofac Trauma Reconstruction 2012;5:115120

Abstract
Keywords

trauma
midface
superior orbital ssure
syndrome
zygomaticomaxillary
complex fracture

Address for correspondence and reprint requests Heath H. Evans,

D.D.S., Oral and Maxillofacial Surgery, Nassau University Medical
Center, 2201 Hempstead Turnpike, Box 72, East Meadow, New York
11554 (e-mail: hevans@numc.edu).

Superior orbital ssure syndrome is an infrequently encountered entity with a unique

presentation and signicant morbidity. This article reviews the background of the
syndrome, treatments in the literature, and discusses a recent case with treatment
strategy.

Superior orbital ssure syndrome (SOFS) is an interesting

symptom complex, which poses difcult questions for the
treating physicians. SOFS can arise from multiple etiologies
and mechanisms. Presented in the following is a review of a
recent traumatic incident confounded by SOFS.

Case Presentation
A 44-year-old man, status-post fall down eight concrete steps,
was transported to the Nassau University Medical Center
Emergency Department by emergency medical services and
presented with a Glasgow Coma Scale of 13. Advanced Trauma
Life Support protocol was followed. Neurosurgery service was
consulted for a subdural hematoma, the Oral and Maxillofacial
Surgery service was consulted to evaluate and treat multiple
facial fractures and lacerations, and the Ophthalmology service
was consulted to assess any visual disturbances resulting from
the periorbital injuries. The patient was admitted to our
institution on the Trauma service. The patient denied any
medical or surgical history. He also reported taking no medications and having no known drug allergies or sensitivities. His
social history was pertinent for alcohol consumption, but the
patient denied tobacco or illicit drug use.
On initial head and neck physical examination, the patient
displayed left periorbital edema and ecchymosis, left lid

received
December 11, 2011
accepted after revision
January 17, 2012
published online
May 10, 2012

Kevin J. Penna, D.D.S. 1

ptosis, limited mandibular range of motion, a palpable step

at the left infraorbital rim, and decreased left facial projection
(Fig. 1). The ophthalmologic examination revealed no acute
decit in visual acuity, minimally elevated left intraocular
pressure (left: 21 vs. right: 17) and anisocoria with the left
pupil dilatated to 5 mm versus the right at 3 mm. Also noted
was an intact afferent pupillary response, paresthesia of the
left frontal region, full restriction of motion of the left globe in
all elds of gaze, and forced duction test was negative for
entrapment of the extraocular muscles (Fig. 2). Further
ophthalmologic evaluation demonstrated no evidence of
optic nerve edema, neuropathy, or retinal detachment.
Imaging included a maxillofacial computed tomography
(CT) which revealed comminuted fractures of the anterior,
posterolateral, and posteromedial walls of the left maxillary
sinus with air uid levels and a hematoma. In addition,
fractures of the left orbital roof and lateral and inferior walls
were noted. The globes were found to be intact, with no
denitive evidence of muscle entrapment. However, disruption of the left superior orbital ssure was found (Figs. 3
and 4).
Subsequently, the diagnosis was made of a left zygomaticomaxillary complex (ZMC) fracture with associated SOFS
caused by compression of the ssure by bony segments. After
discussion of treatment options, an open reduction with

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DOI http://dx.doi.org/
10.1055/s-0032-1313363.
ISSN 1943-3875.

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Figure 1 Initial presentation of the patient s/p fall. Note the typical
presentation of the superior orbital ssure syndrome.

internal xation of the left ZMC fracture was performed

under general anesthesia using lateral brow and a maxillary
vestibular incision with hopes of minimizing the bony impingement of the superior orbital ssure. The patient was
given a perioperative dexamethasone taper beginning with
an immediate preoperative dose of 10 mg. A postoperative
maxillofacial CT was obtained to evaluate the reduction and
reassess the left superior orbital ssure (Figs. 5 and 6). The
patient was followed weekly by the Oral and Maxillofacial
Surgery service as an outpatient. The patient's SOFS resolved
completely (Fig. 7).

Figure 2 Clinical examination photos documenting ophthalmoplegia

of the left eye.

Discussion
SOFS is an infrequently described and reported symptom
complex. According to Kurzer and Patel, the syndrome was
rst described by Hirsceld in 1858.1 SOFS consists of the
following signs: ptosis of the upper eyelid, proptosis of the
globe, ophthalmoplegia, xation and dilatation of the pupil,
and anesthesia of the upper eyelid and forehead.2
The superior orbital ssure serves as a pathway that allows
communication between the orbit and the middle cranial
fossa.3 It lies at the apex of the orbit, bounded medially by the
lesser wing of the sphenoid, inferiorly and laterally by the
greater wing of the sphenoid, and superiorly by the frontal
bone.3 The ssure is reported to be 3  22 mm4 and transmits the oculomotor, trochlear, and abducens nerves (cranial
nerves III, IV, and VI), as well as the rst three branches of the
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Figure 3 Maxillofacial computed tomography scan:, axial cut, bony

window, at the level of the zygomatic arches showing left displaced
zygomaticomaxillary complex fracture.

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Evans et al.

Figure 4 Enhanced view of the left superior orbital ssure from the
previous image. Note the constriction and impingement of the
superior orbital ssure.

trigeminal nerve: the frontal, lacrimal, and nasociliary

nerves.3,8 Also contained in the ssure is the inferior and
superior ophthalmic veins as well as sympathetic laments
from the cavernous plexus.3 (Fig. 8).
Numerous etiologies of the syndrome have been reported
in the literature including syphilis, craniofacial fractures,
hematoma of the cavernous sinus or retrobulbar space,
infection, neoplasm, aneurysm of the internal carotid artery
or arteriovenous stulae, or idiopathic etiologies.18 Regardless of the etiology, the clinical symptoms are primarily the
result of inammation and compression of adjacent nervous
Figure 6 Comparison of the pre- and postoperative maxillofacial
computed tomographic scans. Both images are axial cuts, bony
windows, at the approximate level of the superior orbital ssure. Note
the second image demonstrating widening of the superior orbital
ssure, veried by radiological report, with decreased bony compression and excellent reduction of the fracture segment.

Figure 5 Postoperative maxillofacial computed tomography showing

reduction of the left zygomaticomaxillary complex fractures.

tissue.5 Lid ptosis is caused by either the involvement of the

sympathetic bers arising from the cavernous sinus, resulting
in loss of tone of Mueller muscles, or the involvement of the
somatic efferent bers that course along the superior branch
of the oculomotor nerve, resulting in loss of tone of the levator
palpebrae superioris muscle.3,5 The ophthalmoplegia is secondary to impairment of cranial nerves III, IV, and VI.18
Disturbance of the lacrimal and frontal nerves leads to
anesthesia of the forehead and upper eyelid.3,5 Compromise
of the parasympathetic innervation, which travels with the
oculomotor nerve, results in paralysis of the pupillary ciliary
muscle. This paralysis causes dilatation, xation, and loss of
accommodation of the ipsilateral pupil.3,5,6 The proptosis can
be attributed to the loss of tone of the extraocular muscles
which normally exert a retracting force on the globe.3,5 A loss
or disruption of visual acuity signals involvement of the optic
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Figure 7 Postoperative clinical photos. Note the resolved periorbital

edema and ecchymosis, complete resolution of anisocoria, and normal
ocular movement.

nerve and when concomitant with SOFS is representative of

orbital apex syndrome, rst described by Kjoer, as reported
by Kurzer and Patel.1
Treatment of SOFS remains poorly dened. Most authors
agree that exploration is warranted in cases of neoplasm,
physical impingement, infection, or retrobulbar hemorrhage,2,57 however, traumatic etiologies remain troublesome for the clinician. Although relatively few cases of SOFS
exist in the literature, one author cited an incidence of 1 in
130 cases of LeFort II-III fractures6 at his institution. The
occurrence of optic neuropathy is estimated between 0.5 and
5% of closed head traumas.9 Another author cited a SOFS
incidence of 0.3% over a 14-year period.8 Based on the

literature, open reduction and internal xation of associated

facial fractures may be benecial and result in improvement
of symptoms.3 If the SOFS is secondary to facial trauma, a
complete or partial recovery can be expected without any
intervention aimed at the ssure itself1,3,6 as long as the
nerves are intact. The prognosis is obviously poor if the
nerves have been severed or severely damaged by fractured
bones.1 Also, varying doses of systemic corticosteroids have
been advocated as treatment alone, or in conjunction with
other modalities such as facial fracture reduction.3,4,7,8 One
institution uses dexamethasone with a loading dose of 1 mg/
kg followed by 0.5 mg/kg that is tapered postoperatively3
after reduction of the fractures. Some authors advocate
megadose steroid therapy on the order recommended by
the 2nd National Acute Spinal Cord Injury Study.2 This
involves dosing methylprednisolone 30 mg/kg followed by
5.4 mg/kg/h.10 The benets of steroids appear to be from the
antioxidant mechanism and/or the ability of such high doses
to reduce edema and subsequent ischemia at the affected
sites.11 Regardless of treatment, SOFS seems to improve or
resolve within 6 months, with a plateau of nerve function
recovery occurring at this time,28 unless there is a physical
obstruction impeding recovery. There is, however, one case in
the literature reviewed that documents a SOFS developing
after open reduction and internal xation of facial fractures,
although the patient appeared to be anatomically unique
with a narrow ssure.4
A case of facial trauma, specically a ZMC fracture, complicated by SOFS is presented. The patient was treated with
routine open reduction with internal xation of fractures via
the standard approaches in our institution. No specic instrumentation directly aimed at the superior orbital ssure
was performed. Although we do not know whether the
patient in this case would have experienced symptom resolution without surgical intervention as the literature suggests
and discussed previously,13 it is clear that routine surgical
treatment of ZMC fractures can have a positive effect on the
superior orbital ssure if narrowed due to trauma and may at
least hasten the resolution of SOFS in selected cases. In
addition, the presence of SOFS in the setting of acute orbitofacial fractures, likely due to impingement of the structures of
the superior orbital ssure by bony fragments or increasing
edema, one should consider perioperative dexamethasone
(not necessarily mega dose) administration and routine open
reduction with internal xation of the associated fractures in
an attempt to reestablish proper dimensions of the superior
orbital ssure. This case illustrates one treatment option for
such cases and may provide useful information for clinicians
and patients alike regarding outcomes.

References
1 Kurzer A, Patel MP. Superior orbital ssure syndrome associated

Figure 8 Anatomy of the superior orbital ssure and its contents.

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1979;64(5):715719
2 Acartrk S, Sekolu T, Kesikts E. Mega dose corticosteroid
treatment for traumatic superior orbital ssure and orbital apex
syndromes. Ann Plast Surg 2004;53(1):6064

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Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of
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